The patients with chronic pelvic pain (CPP) experience unrelenting pain and urgency for voiding (hypereflexsive bladder) leading to poor quality of life. The NIDDK has calculated that CPP is responsible for 4,137,000 outpatient or clinic visits/year and about 90% of them are female. Recent study indicates that estimated medical cost for treating CPP exceeds $2 billion/year. The etiology of CPP is complex and difficult to understand. The pain arises due to dysfunction and/or inflammation of any of the pelvic structures including the urinary bladder (cystitis), hindgut (colitis, irritable bowel syndrome), uterus (fibroid and endometriosis) and prostrates (prostatitis) often overlaps to other pelvic and surrounding somatic structures. One of the risk factors for CPP is early episode of urinary tract infection (UTI). The intense painful stimulus and inflammation of the urinary bladder in the neonatal period may adversely affect the neurological development leading to CPP in adulthood. The underlying pathophysiology due to early-life inflammation could be entirely different from that of adults not subjected to any early-life episode and thus warrants further investigation. A systematic study will have significant clinical impact by implementing diagnostic biomarkers, effective prevention strategies and the development of therapeutic intervention. The inhibitory neurotransmitter g-amino butyric acid (GABA) plays a critical role in the pain modulation and lack of its function facilitates chronic pain. Very little is known about how the development of GABAergic system is affected due to neonatal noxious stimulus. A long- lasting pain condition due to early-life episodes may result in transcriptional and/or translational alteration in neurotransmitters and receptor expressions resulting altered neuronal functions, morphology and synaptic connections in adulthood. Although it is largely unknown how such changes in gene expressions induce chronic pain, recent evidence strongly suggests an important role for micro RNAs (miRNAs, small non-coding RNAs) in the cellular plasticity. We hypothesize that the long-lasting spinal sensitization following intense painful visceral stimulus in early-life involves miRNA-mediated posttranscriptional deregulation of developing GABAergic pathway in neonates. The loss of GABAergic tone could be due to (1) lack of GABA synthesis (downregulation of GABA synthesizing enzymes gad1 and/or gad2), (2) downregulation of GABAA receptor subunits (and (3) downregulation of K+, Cl- co- transporter 2 (KCC2) and vesicular GABA transporter (VGAT) in the spinal cord. The proposed study is the first systematic investigation of intrinsic neuromolecular mechanism involved in altered GABAergic tone contributing to CPP in adulthood.